Rheumatoid arthritis (RA) is now recognised as the end point of a disease continuum. Anti-citrullinated peptide antibodies (ACPA) mark the presence of RA-related systemic autoimmunity, but the production of auto-antibodies alone is not sufficient to develop disease. Data on progression between the stages of RA disease are limited, but accumulating evidence suggests a microbial dysbiosis in the gut may trigger RA development. Using a prospective ‘at-risk’ cohort of ACPA positive individuals without arthritis, we investigated for the presence of a gut dysbiosis before the onset of RA.


Faecal samples from 25 ACPA-positive individuals, with non-specific musculoskeletal pain, were sequenced using16S rRNA gene. A control population was selected from publicly available data on the NCBI database, matched for rRNA V4 amplification region, sequencing technique, and approximately for age, gender, diet and ethnicity. Taxonomic analysis was performed using QIIME and MEGAN, and statistical analysis using R software.


Comparison of the ACPA-positive and control populations shows large clustering at bacterial family level. The ACPA population has an abundance of Lachnospiraceae, Helicobacteraceae, Ruminococcaceae, Erysipelotrichaceae and Bifidobacteriaceae, and a lower abundance of Bacteroidaceae, Barnesiellaceae, Methanobacteriaceae amongst others. The relative abundance of bacterial taxa between the ACPA positive and control population was significantly different (P value 0.01, permutation MANOVA).


The gut microbiome of individuals ‘at-risk’ of developing RA is distinct from heathy controls. These pilot data can inform further studies, and are an important step in the attribution of causality to the gut microbiome in the development of RA.


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